II - Acute and Chronic Inflammation Flashcards Preview

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Flashcards in II - Acute and Chronic Inflammation Deck (67)
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1
Q
It is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.
A
Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.31
2
Q
Inflammation which is characterized by plasma protein exudation and a predominantly neutrophilic leukocyte accumulation.
A
Acute inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
3
Q
Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and fibrosis.
A
Chronic inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
4
Q
Five cardinal signs of inflammation?
A
Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.32
5
Q
Initial vascular response to injury?
A
Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33
6
Q
An ultrafiltrate of blood which contains little protein. Results from arteriolar vasodilation and increased blood flow.
A
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
7
Q
Results from increased vascular permeability, leading to leakage of protein into tissues.
A
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
8
Q
Fluid accumulation in extravascular space.
A
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.34
9
Q
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling
A
Selectins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
10
Q
State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion
A
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
11
Q
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration
A
PECAM-1/CD 31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
12
Q
State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion
A
ICAM -1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
13
Q
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin
A
Sialyl-Lewis X modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
14
Q
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin
A
Sialyl-Lewis X-Modified glycoprotein(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
15
Q
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1
A
Integrins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
16
Q
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31
A
CD-31(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.37
17
Q
The process of luekocyte accumulation at the periphery of blood vessels is called ______.
A
Margination(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.36
18
Q
Arrange the following steps in the inflammatory response:A. Recruitment of leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. Resolution
A
C, A, D, B, E(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
19
Q
Arrage the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion
A
C, B, D, A(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.35
20
Q
Process of coating microorganisms with proteins that facilitate phagocytosis.
A
Opsonization(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.38
21
Q
A lymphocyte with ingested microorganism fused with lysosome is called _______.
A
Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.39
22
Q
The most important lysosomal enzyme involved in bacterial killing.
A
Elastase(TOPNOTCH)
23
Q
Process of leukocyte migration toward sites of infection or injury along a chemical gradient.
A
Chemotaxis(TOPNOTCH)
24
Q
The most important lysosomal enzyme involved in bacterial killing.
A
Elastase(TOPNOTCH)
25
Q
A peptide Leukocyte granule constituent which kills microbes by creating holes in their membranes.
A
Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40
26
Q
Predominant form of leukocyte during the first 6 - 24 hours of inflammation?
A
Neutrophils(TOPNOTCH)
27
Q
Predominant form of leukocyte during 24-48 hrs after the onset of inflammation?
A
Monocytes(TOPNOTCH)
28
Q
Substances responsible for leukocyte-induced tissue injury?
A
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
29
Q
Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1 leading to impaired leukocyte adhesion and migration through endothelium.
A
Leukocyte adhesion deficiency type 1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
30
Q
Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.
A
Leukocyte adhesion deficiency type 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
31
Q
Results from a defect in the protein involved in membrane docking and fusion.
A
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
32
Q
NADPH deficiency or defect resulting in decreased oxidative burst.
A
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
33
Q
Type of acute inflammation characterized by the outpouring of watery, relatively protein-poor fluid derived from the serum or endothelial lining of peritoneal, pleural, and pericardial cavities.
A
Serous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
34
Q
Fluid in a serous cavity is called ______.
A
Effusion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.43
35
Q
This type of inflmmation results from greater vascular permeability that allows larger molecules to pass the endothelial barrier.
A
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
36
Q
Histologically, appears as an eosinophilic meshwork of threads or sometimes an amorphous coagulum.
A
Fibrinous inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
37
Q
This type of inflammation is manifested by the presence of large amounts of purulent exudate consisting of neutrophils, necrotic cells, and edema fluid.
A
Suppurative (purulent) inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
38
Q
Focal collections of pus that may be caused by seeding pyogenic organisms into a tissue or by secondary infections of necrotic foci.
A
Abscess(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
39
Q
It is an excavation of the surface of an organ or tissue that is produced by necrosis of cells and sloughing of inflammatory necrotic tissue.
A
Ulcer(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.44
40
Q
Vasoactive amines that are preformed molecules in secretory granules of mast cells, basophils and platelets.
A
Serotonin, Histamine(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
41
Q
Complement fragments which are anaphylotoxins.
A
C3a, C5a (A for anaphylotoxin)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
42
Q
Complement fragment which aids in opsonization.
A
C3b (b for binding)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
43
Q
Membrane attack complex
A
C5b, C6-9(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
44
Q
It is the cytolytic endproduct of the complement cascade, which forms a transmembrane channel causing osmotic lysis of target cells.
A
Membrane attack complex (C5b,C6-9)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.46
45
Q
Enzyme blocked by NSAIDS.
A
Cyclooxygenase 1 and 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
46
Q
Enzyme inhibited by glucocorticoids
A
Phospholipase A2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.47
47
Q
Polypeptide products of many cell types that function as mediators of inflammation and immune response.
A
Cytokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
48
Q
They are a family of small structurally related proteins that act primarily as chemoattractants for different subsets of leukocytes.
A
Chemokines(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
49
Q
Major cytokines in acute inflmmation.
A
TNF and IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.48
50
Q
A short-lived, soluble, free-radical gas produced by endothelial cells causing smooth muscle relaxation and vasodilation.
A
Nitric oxide(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.49
51
Q
This component of the coagulation cascade initiates four systems involved in the inflammatory response, namely the kinin, clotting, fibrinolytic and complement systems.
A
Activated Hageman Factor / Factor XIIa(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.52
52
Q
Inflammation characterized by infiltration with mononuclear cells, tissue destruction and repair involving angiogenesis and fibrosis.
A
Chronic Inflammation(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.53
53
Q
Macrophages in the liver
A
Kupffer cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
54
Q
Macrophages in the spleen and lymph nodes
A
Sinus histiocytes(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
55
Q
Macrophages in the CNS
A
Microglial cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
56
Q
Macrophages in the lungs
A
Alveolar Macrophages(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.54
57
Q
A focus of epiheloid cells, rimmed by fibroblasts, lymphocytes, histiocytes, occasional giant cells.
A
Noncaseating tubercle, Tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
58
Q
Central amorphous granular debris, loss of all cellular detail, acid-fast bacilli
A
Caseating tuberculosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
59
Q
Acid-fast bacilli in macrophages, noncaseating granulomas
A
Leprosy(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
60
Q
Microscopic to visible lesion, enclosing wall of histiocytes, plasma cell infiltrates, necrotic central cells without loss of cellulr outline
A
Gumma (Syphilis)(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
61
Q
Rounded or stellate granuloma containing central granular debris and recognizable neutrophils, giant cells uncommon.
A
Cat-scratch Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
62
Q
Noncaseating granulomas with abundant activated macrophages
A
Sarcoidosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
63
Q
Occasional noncaseating granulomas in intestinal walls, with dense chronic inflammatory infiltrate
A
Chron disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
64
Q
Cells with pink, granular cytoplasm with indistinct boundaries.
A
Epitheloid cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
65
Q
40-50 um in size, consisting of a large mass of cytoplasm and many nuclei.
A
Giant cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
66
Q
Necrotic material which appears amorphous, structureless, granular debris, with complete loss of cellular details.
A
Caseous necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.56
67
Q
Cytokines which stimulate prostaglandins in the hypothalamus, producing fever.
A
TNF, IL-1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.57

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